BackgroundIvabradine is a novel specific heart rate (HR)-lowering agent that improves event-free survival in patients with heart failure (HF).ObjectivesWe aimed to evaluate the effect of ivabradine on time domain indices of heart rate variability (HRV) in patients with HF.MethodsForty-eight patients with compensated HF of nonischemic origin were included. Ivabradine treatment was initiated according to the latest HF guidelines. For HRV analysis, 24-h Holter recording was obtained from each patient before and after 8 weeks of treatment with ivabradine.ResultsThe mean RR interval, standard deviation of all normal to normal RR intervals (SDNN), the standard deviation of 5-min mean RR intervals (SDANN), the mean of the standard deviation of all normal-to-normal RR intervals for all 5-min segments (SDNN index), the percentage of successive normal RR intervals exceeding 50 ms (pNN50), and the square root of the mean of the squares of the differences between successive normal to normal RR intervals (RMSSD) were low at baseline before treatment with ivabradine. After 8 weeks of treatment with ivabradine, the mean HR (83.6 ± 8.0 and 64.6 ± 5.8, p < 0.0001), mean RR interval (713 ± 74 and 943 ± 101 ms, p < 0.0001), SDNN (56.2 ± 15.7 and 87.9 ± 19.4 ms, p < 0.0001), SDANN (49.5 ± 14.7 and 76.4 ± 19.5 ms, p < 0.0001), SDNN index (24.7 ± 8.8 and 38.3 ± 13.1 ms, p < 0.0001), pNN50 (2.4 ± 1.6 and 3.2 ± 2.2 %, p < 0.0001), and RMSSD (13.5 ± 4.6 and 17.8 ± 5.4 ms, p < 0.0001) substantially improved, which sustained during both when awake and while asleep.ConclusionOur findings suggest that treatment with ivabradine improves HRV in nonischemic patients with HF.

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Behçet's disease (BD) is a multisystemic disorder characterized by endothelial dysfunction. However, the relationship between oxidative stress and endothelial function has not been clearly shown. We investigated the relationship between oxidative stress markers and endothelial function in patients with BD. Patients with BD (n = 40) having active disease and sex- and age-matched 40 controls were included. Endothelial function was assessed by flow-mediated dilatation (FMD) technique. Serum gamma-glutamyltransferase (GGT) and high-sensitive C-reactive protein levels (hsCRP) were measured in all participants. Brachial artery FMD was significantly lower in patients with BD than in controls. Gamma-glutamyltransferase and hsCRP levels were higher in patients with BD than in controls. Also, GGT and hsCRP levels were inversely correlated with endothelial function. Oxidative stress markers are elevated in patients with BD having active disease. This may be one of the reasons behind the vasculitis in active BD.

Non-dipper hypertension is associated with increased cardiovascular morbidity and mortality. We aimed to evaluate serum gamma-glutamyl transferase (GGT) level, which is accepted as a marker for oxidative stress and its relationship with inflammatory activity in patients with non-dipper hypertension. Age and sex matched 43 dipper hypertensive patients, 40 non-dipper patients, and 46 healthy subjects were included into the study. Serum GGT and C-reactive protein (CRP) levels were measured and compared between each of the groups. Serum GGT activity was higher in the non-dipper and the dipper hypertensive groups than in the control group (33.5 ± 11.8 and 28.1 ± 10.1 U/l, respectively, vs. 21.2 ± 6.5 U/l; p < 0.001). There was a statistically significant difference in serum GGT activity between the non-dippers and the dippers (p = 0.021). When compared with the control group, serum CRP levels were significantly increased in both the non-dipper and the dipper hypertensive groups (6.1 ± 2.6 and 5.4 ± 2.1 mg/l, respectively, vs. 2.8 ± 1.7 mg/L; p < 0.001). Increased CRP levels were higher in non-dippers than dippers (p = 0.046). A significant correlation was found between GGT and CRP measurements (r = 0.37, p = 0.002). Serum GGT levels, which are markers of the oxidative stress and CRP levels, are both increased in non-dipper hypertension. Increased GGT activity, found to be correlated with CRP levels, may be one of the reasons behind the non-dipper hypertension related cardiovascular complications.